TB MENINGITIS

SUBMITTED BY SUBMITTED TO

[Link] M S Mrs. INDRA

1I yr. [Link] NSG Professor

SRMCN SRMCN

Submitted on:12-2-12
PATIENT PROFILE

Name : Baby Amoolya

Age : 1 ½ yr.
Sex : Female
Hospital No : 66897
Religion : Hindu
Ward : PICU
Hospital : RAPCC
Diagnosis : Tuberculous Meningitis with
hydrocephalus
Date of admission : 16/2/2012

CHIEF COMPLAINTS
Baby Amoolya , a 1 ½ year old female child was brought to RAPCC with complaints
of cold, cough and fever for the last 7 days and also had vomiting since 3 days; at the time of
admission. They gave some medicines for fever which worked but the day before admission
again baby had high temperature. She got vomiting also which was non blood stained, non
bilious. Cough was also non proactive. After admission on 17 th she got seizures with
unrolling of eye, tonic posturing of both upper limbs followed by drowsiness. Fever was
persisting and she had one episode of vomiting after seizures. Glasgow coma scale rate was
11/15 (E4 M5 V2).
Her Hb was 8.0gm% and in urine culture there were numerous pus cells, Heavy
growth of klebisella and candida on 18th December 2009 they did a lumbar puncture and CFS
was checked. This showed a protein content of 120.3, cell count-800, RBC-3600. Again on
26/12/2009 they did a CT head which revealed communicating hydrocephalus. (VS1-44%).
She is also showing extra pyramidal movements. She was diagnosed as having tuberculosis
meningo-encephalitis with hydrocephalus and also thrombocytopenia with extra pyramidal
movements.
PAST MEDICAL HISTORY
She had a history of fever before this episode, which was treaed and cured. Also
history of ear discharges for one month before the admission no previous surgical history or
any accidents or injuries. She had a history of TB contact, open case of TB (Mother’s sisters).
FAMILY HISTORY
Dead
Patient

Female

FAMILY MEDICAL HISTORY

Her father died 3 years ago, whose cause is unknown to mother. Her mother’s sister is
an open case of TB and she is in close contact with the baby.

BIRTH HISTORY
a) Antenatal History
Her mother had an arranged marriage. Mother said, they did have some usual health
problems and would take treatment avoiding to their socioeconomic condition. She had
and irregular or antenatal check up. She is illiterated and she is a Cooley so she does not
know whether TT and iron and folic acid tablets was taken, No history of RHO
incompatibility.

b) Natal History
Mother had a normal vaginal delivery and Baby Amoolya was a term baby, which
was delivered in Lady Goshen government hospital.
c) Post Natal History
Baby cried soon after the birth. Birth weight was 2.1 kg. Breastfeeding was begun 1 ½
hrs after delivery.
IMMUNIZATION HISTORY

Immunization Dose Taken/not taken

BCG, OPV At birth, O dose (OPV) Take
OPV, DPT (6 week) 1st dose Taken
OPV, DPT (10 week) 2nd dose Taken
OPV, DPT (14 week) 3rd dose Taken
DIET HISTORY
Baby Amoolya was on exclusive breast feeding till 8 months. Weaning was started at
the age of 8 months. Now on ryles tube feeding (cooled milk and )
PERSONAL HISTORY
Sleeping pattern was regular before getting fever but now she has body pain and she
tries to sleep but when someone touches her, she urinates because of pain. She passes
motion and urine regularly.
SOCIO ECONOMIC STATUS
Baby Amoolya’s family is a joint family, she lives with her grandparents, mothers
sister and husband and mother’s brother. Her mother is a daily wager who earns about Rs.
1500/- They usually go to hospital if they have enough money for treatment otherwise do
self treatment.
VITAL SIGNS
Temperature - 1020F
Pulse – 126/mt
Respiration – 28/mt
Blood pressure – 100/50mm Hg

PHYSICAL EXAMINATION

General appearance : Thin

Level of activity : Dull
Emotional stability : Irritable
Level of consciousness : Semiconscious

Face
Normal facial features. No edema or puffiness an the face.

Eyes
Visual acuity : Normal
Corneal reflex : Present
Conjunctiva : Normal
Pupil : Reacting to light
 Eye lid : Normal. No presence of ptosis /edema/furuncles or
chalezions
Eye ball : Slightly sunken
Lacrimal apparatus : Patency is normal, palpable
Sclera : No discoloration
Cornea : No ulceration or opacities present
Ears
Discharge : Not present. But she has a history of ear
discharge one month back
Position : Normal
Hearing : Not much responding. Most of the time she is
Drowzy and lethargic. But sometimes, when her name
is called she stares.
Skin
Colour : Dark
Turgor : Normal
Lesions : Skin break-down present where the chest
Electrodes where present and also at the right side of the
neck where control line was present
Texture : Smooth
Nose
Shape and size : Normal
Septum : Normal
Discharge : Absent
Nostril : Patent
Ryles tube present on her left nostril
Mouth
Lips : Dry lips sometimes bleeding also present
Teeth : 7 teeth
Dental caries : No
Gums : normal
Tongue : White coated oral thrush present
Head
Hair distribution : Well, hairy
 Fontanel : Closed, anterior fontanelle slight bulging present
She is diagnosed as having communicating hydrocephalus
Neck
Movement : Nuchal rigidity present
Trachea : Central
Thyroid : Not enlarged
Neck vein : Distended
Palpation : No lymph node is palpable
Chest and lungs
Inspection
Chest symmetry : Normal
Size : Asymmetry
Shape : Pigeons chest
Retractions present
Palpation : The sternum can be palpable
Auscultation : No wheezing
GROWTH AND DEVELOPMENT OF BABY AMOOLYA
MEASUREMENT FINDINGS NORMAL REMARKS
Height 77 cm 80-90cm (by 2 years) Almost normal
Weight 7.6 kg 10-12 kg (by 2 years) Weight is less than normal
Head circumference 44 cm 35 cm Normal
Chest circumference 46 cm Normal
MAC 12 cm Normal
Abdominal girth 40 cm Normal

DEVELOPMENT
CRITERIA’S BOOK PICTURE PATIENT REMARK
PICTURE
Gross Motor Assumes at 15 months Yes All the gross motor
1. Able to stand development was
without help normal before the
2. Able to creep Assumes by 15 month Yes, she was diagnosis of the
upstairs able disease but now she is
 3. Able to kneel with Assumes by 15th month Yes not able to perform
support -do- Yes any of these activities.
4. Able to assume
standing position Assumes by 18th month Yes
without supper
5. Can throw ball with Assumes by 18th month Yes
out falling
6. Able to run but palls Assumes by 18th month Yes
often
7. Able to walk
upstairs with one Assumes by 18th month Yes
hand held
8. Able to pull and - -
push toys
9. Able to jump up - -
place with both feet
10. Able to sit in a chair Assumes by 18th month Yes
11. Able to go upstairs
with both feet -
-
FINE MOTOR
Gross Motor Assumes at 15 months Yes All the gross motor
1. Scribbles development was
spontaneously normal before the
2. Constantly casting Assumes by 15 month Yes diagnosis of the
objects on the floor disease but now she is
3. Able to use cup well Assumes by 18h month Not so not able to perform
4. Turns pages of a correctly any of these activities.
book 2-3 at a time Assumes by 15 month Yes
5. drawing makes
contents strokes -do-
 CENTRAL NERVOUS SYSTEM INFECTION
Acute infection of the central nervous system (CNS) is the most common cause of
fever associated with signs and symptoms of CNS disease in children. Infection may be
caused by virtually any microbe, the specific pathogen being influenced by the age and
immune status of the host and the epidemiology of the pathogen. In general, viral infections
of the CNS are much more common than bacterial infections, which in turn, are more
common than fungal and parasitic infection.
Regardless of etiology, most patients with acute CNS infection have similar clinical
syndromes common symptoms include headache, nausea, vomiting anorexia, restlessness and
irritability. However most of these symptoms are nonspecific common signs of CNS
infection, in addition to fever, include photophobia, neck pain and rigidity, obtundation,
stupor, coma, seizures, and focal neurological deficits. The severity and constellation of signs
are determined by the specific pathogen, the host, and the are of the CNS affected. Infection
of the CNS may be diffuse or focal. Meningitis and encephalitis are examples of focal.
Meningitis implies primary involvement of the meninges, where as encephalitis indicates
brain parenchyma involvement.
Because these anatomic boundaries are often not distinct, many patients have
evidence of both meningeal and parenchyma involvement and should considered to have
meningeoencephalitis.
TUBERCULOUS MENINGITIS
Meningitis is the most common infection of the CNS. It can be caused by a variety of
organisms, but the three main types are the following.
1. Bacterial or pyogenic, caused by pus forming bacteria, especially the meningococcal,
pneumococcal and haemophilus organisms.
2. Tuberculosis, caused by the tubercle bacillus
3. Viral or aseptic, caused by a wide variety of viral agents.
Meningitis is a serious complication of childhood tuberculosis. It may occur at any
age, but is most common between 6 and 24 months of age, there is usually a focus of primary
infections with tuberculosis or concomitantly with miliary tuberculosis. Mortality rate has
reduced but survivors may be left with serious disabling neurological sequelae.
Tuberculosis meningitis is mycobacterium tuberculoses infection of the meninges the
system of membranes which envelops the central nervous system. It is the most common
form of CNS tuberculosis.
Etiology
There are five closely related mycobacterium in the mycobacterium tuberculosis complex: M.
Tuberulosis, M. bovis, M. Africanum, M. microti, and M. Canetti. All belong to the order
actinomycetales and the family Mycobacterialeae. M. Tuberculosis is the most important
cause of tuberculosis disease in humans. The tubercle bacilli are non-spare-forming, non
motile, pleomorphic, weakly gram-positive curved rods 2-4 mm specimens or culture media.
They are obligate aerobes that grow in synthetic media containing glycerol as the carbon
sourer and ammonium salts as the nitrogen source and ammonium salts as the nitrogen source
(eg: Lowenstein jensen culture media). These mycobacterium grow best at 37-51 0c, produce
niacin and lack pig mention.
Transmission
Transmission of M. Tuberculosis is person to person, usually by airborne mucus
droplet nuclei, particles 1-5 mm in diameter that contain M. Tuberculosis. Transmission
rarely occurs by direct contact with an infected discharge or a contaminated fomite. The
chance of transmission increases when the patient has an acid-fast smear of sputum, an
extensive upper tube to filtrate or cavity, copious production of thin sputum, and sever and
forceful cough. Environmental factors, especially. Poor air circulation, enhance transmission.
Most adults no longer transmit the organism within several days to 2 week after beginning
adequate chemotherapy, but some patients remain infections for many weeks.
Young children with tuberculosis rarely infect other children or adults. Tubercle
bacilli are sparse in the endo-bronchial secretions of children with pulmonary tuberculosis,
and cough is often absent or lacks the tussive force required to suspend infections particles of
the correct size. However, children and adolescents with adult-type pulmonary tuberculosis
can transmit the organism. Airborne transmission of M. bovis and M. Africanum can also
occur. Mr. bovis may penetrate the gastrointestinal mucosa or invade the lymphatic tissue of
the oro-pharynx when large numbers of the organism are ingested. Human infection with M.
bovis is rare in developed countries as a result of the pasteurization of milk and effective
tuberculosis control programs for cattle.
Pathogenesis
The primary complex of tuberculosis includes local infection at the portal if entry and
the regional lymph nodes that drain the area. The lung is the portal of entry in over 98% of
cases. The tubercle bacilli multiply initially within alveoli and alveolar ducts. Most of the
bacilli are killed, but some survive within nonactivated macrophages, which carry them
through lymphatic vessels to the regional lymph nodes when the primary infection is in the
lung, hilar lymph nodes usually are involved, although an upper lung focus may drain in to
Para tracheal nodes. The tissue reaction is the lung parenchyma and lymph nodes intensify
over the next 2-12 wk as the organisms grow is number and tissue hypersensitivity develops.
The parenchyma position of the primary complex often heals completely by fibrosis or
calcification after undergoing caseous necrosis and encapsulation.
In most cases of initial tuberculosis infection the lymph nodes remain normal in size
however, hilar and Para tracheal lymph nodes that enlarge significantly as a part of the host
inflammatory reaction may encroach on a regional bronchus. Partial obstruction of the
bronchus caused by external compression may cause hyperinflation in the distal lung
segment complete obstruction results in atelectasis. Inflammed caseous nodes can attach to
the bronchial wall and erode through it, causing end bronchial tuberculosis or a fistula tract.
The caseum causes complete obstruction of the bronchus. The resulting lesion, a combination
of pneumonias and atelectasis, has been called a collapse-consolidation or segment lesion.
During the development of the primary complex, tubercle bacilli are carried to most
tissues of the body through the blood and lymphatic vessels. Al though seeding of the organs
of the reticulo-endothelial system is common, bacterial replication is more likely to occur in
organs with conditions that favour their growth, such as the lung apices, brain, kidneys and
bones.
The time between initial infection and clinically apparent disease is variable.
Disseminated and meningeal tuberculosis are early manifestations often occurring within 2-6
months of infection clinically significant lymph node or endobronchial tuberculosis usually
appears within 3-9 month lesions of the bones and joints take several years to develop. Where
as renal lesions may become evident decades after infection. From 25-25% of children with
tuberculosis develop extrapulmoarry manifestations compared with about 10% of immuno
competent adults.
The risk of dissemination of M. Tuberculosis is very high in HIV infected persons.
Pathology
The meningeal surface is covered with yellow grayish exudates and tubercles. These
are most severe at the base, in the region of the temporal lobes and along the courses of the
middle cerebral artery. The subarachnoid space and the arachnoids’ villi are oblitered
resulting in poor reabsorption of cerebrospinal field. This results in dilation of the ventricles
as a consequence of increased cerebrospinal fluid. A gelatinous exudates blocks
cerebrospinal filed pathway and causes hydrocephalus.
On cut section the ventricles are dilated, and the ependyma is inflamed, congested and
granular. The choroids plexus is congested, edematous and studded with tubercles. There is
cerebral edema there may be infracts in the brain due to vascular occlusion. Tuberculous
encephalopathy results in diffuse edema of brain simulating post infective allergic
encephalopathy. Necrotizing or hemorrhagic leukoencephalopathy may occur in some cases.
Clinical manifestations
The majority of children with tuberculosis infection develop no signs or symptoms at
any time. Occasionally, infection is marked by low grade fever and mild cough and rarely
by high fever, cough, malaise and flue like symptoms that resolve within a week the
proportion of extra-pulmonary tuberculosis cases has increased over the past 2 decades in the
U.S about 15% adult tuberculosis cases are extrapulmonary and 25-30% of children with
tuberculosis have an extra pulmonary presentation.
The clinical course of tuberculosis meningitis is described in three stages. This
differentiation is or bitrary as one stage merges into other.
1. Prodromal stage or stage of invasion
The onset is insidious and vague with low grade fever, loss of appetite and
disturbed sleep. The child who was active and playful earlier becomes peevish,
irritable and restless. Vomiting is frequent and older children may complain of
headache child may exhibit head banging and resents exposure to bright sunlight
(photophobia) constipation is usual.
2. Stage of Meningitis
During this stage neck rigidity can be demonstrated and kernings sign is
positive. The temperature is elevated, usually up to 39 oc and may be remittent or
intermittent. The pulse is slow but usually regular in rhythm and volume. Breathing
may be disturbed. The patient may be drowsy or delirious. Muscle tone may be
increased. As the disease progresses, convulsions and neurological deficits like
monoplegia and hemiplegia may occur. The sphincter control is usually lost.
3. Stage of Coma
This stage is characterized by loss of consciousness, rise of temperature and
altered retratory pattern pupils are dilated, often unequal, with nystagmus and squint.
Ptosis and opthalmoplegia are frequent with the progression of the disease the coma
deepens severity. The respiration becomes cheyne-stokes or Biot type, bradycardia is
common un treated illness is lethal is about four weeks.
According to udani et al (1972), the frequency of various neurological
manifestations is as follows hemiplegia (20%) Quadriplegia (19%), monoplegia (3%)
hemiballismus (11%), tremors (6.1%) midline cerebellar syndromes (4%), cranial
 nerve palsies (14%) decerebrate rigidity (13%) decorticate rigidity (3%) and
cerebella. Hemispheric lesions (1.0%)
Risk for tuberculosis infection
 Children exposed to high risk adults
 Foreign born persons from high prevalence countries
 Poor and indigent persons, especially in large cities
 Homeless persons
 Persons who inject drugs
 Present and former residents or employees of correctional institutions,
homeless shatters and nursing homes
 Health workers coring for high risk patients

Risk for progression to tuberculosis disease once infected

 Infants and children ≤4yr of age, especially those <2yr of age
 Adolescents and young adults
 Persons co-infected with HIV
 Persons with skin test conversion in the past 1-2yr incases of malignancy and
solid organ transplantation, immunosuppressive medical treatments, diabetes
mellitus, chronic renal failure, silicosis and malnutrition.
Diagnosis
Lumber puncture
CT scan .
Serological tests
Others
Tests for HIV should be performed on all suspected subjects. X-ray of the chest may
provide supportive evidence for tuberculosis. Tuberculin test should be done.

Prognosis
The prognosis is related to the age of the patient, stage at which diagnoses is made,
adequate of hearken and presence of complications. The prognosis is poorer in younger
children. Early diagnoses, adequate and prolonged therapy improves the prognosis unheard
cases die within 4 to 8 weeks.
Treatment
 The treatment of tuberculosis meningitis should be prompt , adequate and
prolonged for at least 12 months . Short course chemotherapy is not recommended. At least 4
an tubercular drugs should be used for initial 2 months uprising of (1)Isonized (5mglkglday,
maximum 300 mg/day).

2) Reframing (10 mg/kg/orally , once on empty stomach is the morning , maximum dose
600 mg/day .
3) Ethambutol (15-20 mg/ kg / day) or streptomycin (30-40 mg /kg/ day (M) the first
three drugs are further continued to complete one year of therapy.
Steroids
It is desirable to start with parental corticucosteroids
( dexamethasone ) for 1-2 weeks and change to oral drugs ( prednisolone) once brain
edema settles oral corticosteroids may be continued for 6 weeks and tapered over next
two weeks steroids reduce the intensity of cerebral edema , risk of development of
arachnoiditis

Symptomatic therapy
Of raised intracranial pressure, seizures, dyselectrolytemia should be kept
under observation for development of papilla edema, optic atrophy or increasing head
circumference, desecration is common in advanced cases in the acute phase ventriculocanal
shunt may be required in cases with increasing hydrocephalus and persistent reverberation.
Medication
Inj. Prednisolone
Inj. Dexamethasone
Inj. Phenobarbitone
Inj. Flucanazole
Inj. Ciprofloxacin
Investigations
Investigations Findings Normal
Hb 8.0 gm% 12-16
TLC 9530cells/cumm 4000-10000
Platelet 8.13 cells/cumm 150000-400000
Urea 40 mgldl 10-45
 Creatinine 0.3 mgldl 0.4-14
Na+ 139 mmol/l 136-149
K+ 5.6 meq/l 3.5-5.3
Cl- 99 meq/l 98-111
Hlo3 20.1 meq/l 23-27
Total bilirubin 0.4 gm/l 0.2-1.2
SGPT 101 U/L 5-40
Cal 9.4 mg/dl 8.1-104
Urine culture
Numerous pus cells – Heavy growth – Klebsiella, candida

CSF
Vol - 0.3
App - Bld cells
protein - 120.3
cell count - 800
RBC - 3600
GRBs - 125

CT Scan
Communicating hydrocephalus (VSI-44%)
NURSING DIAGNOSES
1. Hyperthermia related to presence of infection / underlying pathology.
2. Impaired physical mobility related to semiconscious stage
3. Imbalanced nutrition less than body requirement related to present disease
condition.
4. Impaired oral mucous membrane related to presence of candidiasis infection
5. Impaired skin integrity related to presence of skin breakdown.
6. Risk for injury related to physical immobility depressed sensorium,
intracranial problem.
7. Acute pain related to presence of the infection
8. Impaired family processer related to a child hospitalized with a potentially fatal
condition.
Assessment Diagnosis Goal  Plan Implementation Evaluation
of action
Subjective data Impaired skin Child will maintain  Inspect skin  Inspected skin
Mother says Childs integrity related to normal skin integrity surfaces regularly surfaces (redness Child’s skin break
skin in getting broken presence to presence for signs of present on the down is healing
in some areas and of skin break down irritation redness pressure points)
sadness in present is  Place the child  Placed the
present on a pressure child on water bed
reducing surface to
Objective data prevent tissue
- child is bed breakdown and
ridden pressure necrosis
- skin break  Change  Changed
down and redness position frequently position 4 hourly
present in the unless
shoulders, ankle contraindicated  Protected
region.  Protect pressure points
pressure points  Gently
 gently massaged the skin
message skin with
lotion or other
lubricating
 substance
Objective data
- seizures  Avoided
present Risk for injury related Child will experience  Avoid stimulation stimulation Child didn’t have any
- TB to physical no seizures that precipitates episode of seizure
Meningitis immobility depressed undesirable activity after that.
Pain present sensorium, responses  Scheduled nursing
intracranial problem  Schedule nursing activities
activities for
minimal
disturbance  Administered
 Administer antiepileptic drugs
antiepileptic drugs as prescribed
as prescribed  Maintained IV
 Maintain IV fluids as
fluides as prescribed
presribed  Pain is relieved as
 Prevent or possible
relive pain since
pain causes
increased ICP
 Hyperthermia related Child will maintain  Assessed the Child maintained
Subjective data to presence to normal body  Asses the vital vital signs of the normal body
Mother says child is presence of temperature signs of the child child temperature.
having high fever infection/underlying especially
since before getting pathology. temperature
 used tepid
and mitted and is still  use tepid
sponging and wild
present sponging for the
sponging
Objective data body and cold
- T – 1020F sponging in the
TB– meningitis axilla and femoral
region
 checked the
 check the
temperature after
temperature after
giving tepid
15mts of giving
sponging
tepid sponging.
 gave
 give medicines
antipyretics and
for hyperthermia
antibiotics
and underlying
pathologic
condition.
 Impaired physical Child will exhibit Child still have the
Subjective data mobility related to proper physical - Assess the - Assess the impaired physical
Mother says child is presence of mobility condition of the condition of the mobility
not able to move or semiconscious stage child for getting child
walk after she had got an base line data
the disease. - Give adequate - Gave adequate
objective data exercise so that motility and
- Child is confined contractures can exercised but
to bed be avoided child has pain
- Semiconscious - Encourage mother - Encouraged
- Seizures present to take the child mother to take
on her lap or on child on her lap
upright
- Change positions - Changed positions
frequently for frequently
avoiding
impairment of
skin
- Treat the Treatment is being
underlying given to the child
disease condition Child is gaining
  Asses the present weight but not so
Imbalanced nutrition Child will receive status of the child  Assessed the high Weight
Subject data less than body optimal nutrition inorder to get a condition of the
Child is not taking requirement related to baseline data child
food and she became present disease  Provide  Cold milk is given
thin condition nourishment in to the child every 2
Objective data manner suitable to hourly
 Thin body child’s condition.  IV fluids are
 Semiconscious  Give IV Fluids or given
 Weight parental therapy as  Recorded intake
prescribed and out put
 Record intake and Weighed the child
output in alter native
 Weigh daily or as days.
ordered
HEALTH EDUCATON
Health education given about importance of giving weaning or fruit juices as possible.
 Proper giving of medicines as prescribed
 Reducing close contact with 7B persons
 Proper hygienic use of cloths and food
 Cleanliness of body and housing surroundings
 Follow up.

CONCLUSION
Baby Amoolya’s health was improved. But she is still leave activity intolerance she
in taking ragie and fruit juices by mouth. She got discharged.

BIBLIOGRAPHY
1. Hockenberry. M., Wong’s essentials of pediatric nursing. 7th edition. Mosby
publications. Pg:807, 1040
2. Behrman. Nelson textbook of pediatrics. 17th ed. Mosby Publication. Pg.906, 2060.
3. Ghai. O.P. essential pediatrics – 6th edition. CBS publications Pg – 520